ArticleThe Journal of biological chemistry2009
T cell receptor signaling co-regulates multiple Golgi genes to enhance N-glycan branching.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 66 citations in OpenAlex.
- Effect of vitamin D supplementation on N-glycan branching and cellular immunophenotypes in MS.Annals of clinical and translational neurology · 2020Trial
- Post-COVID impairment of T cell responses to community-acquired pathogens can be modified by activating cellular metabolism.PLoS pathogens · 2026Article
- Mucosal glycans: key drivers of the development of inflammatory bowel disease and a potential new therapeutic target.Nature reviews. Gastroenterology & hepatology · 2026Review
- Post-COVID impairment of memory T cell responses to community-acquired pathogens can be rectified by activating cellular metabolism.bioRxiv : the preprint server for biology · 2026Article
- Age-related remodeling of the sialoglycans dampens murine CD8Science advances · 2025Article
- Glucose-dependent glycosphingolipid biosynthesis fuels CD8Cell metabolism · 2025Article
- HScience advances · 2024Article
- Elevated level of multibranched complex glycan reveals an allergic tolerance status.Clinical proteomics · 2024Article
- Combinatory glycoengineering of monoclonal antibodies and its application in cancer therapy: a narrative review.Translational cancer research · 2024Review
- Identification of immune subsets with distinct lectin binding signatures using multi-parameter flow cytometry: correlations with disease activity in systemic lupus erythematosus.Frontiers in immunology · 2024Article
- Tumor glucose metabolism and the T cell glycocalyx: implication for T cell function.Frontiers in immunology · 2024Review
- Review
- Dietary glucosamine overcomes the defects in αβ-T cell ontogeny caused by the loss of de novo hexosamine biosynthesis.Nature communications · 2022Article
- The Role of Glycosylation in Inflammatory Diseases.Advances in experimental medicine and biology · 2021Article
- Golgi α1,2-mannosidase I induces clustering and compartmentalization of CD147 during epithelial cell migration.Cell adhesion & migration · 2020Article
- Establishing Rules for Self-Adhesion and Aggregation ofLangmuir : the ACS journal of surfaces and colloids · 2020Article
- Human T cell glycosylation and implications on immune therapy for cancer.Human vaccines & immunotherapeutics · 2020Review
- Tumor-associated carbohydrates and immunomodulatory lectins as targets for cancer immunotherapy.Journal for immunotherapy of cancer · 2020Review
- N-Glycan Branching Decouples B Cell Innate and Adaptive Immunity to Control Inflammatory Demyelination.iScience · 2020Article
- Altered Cell Surface N-Glycosylation of Resting and Activated T Cells in Systemic Lupus Erythematosus.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
T cell receptor (TCR) signaling enhances beta1,6GlcNAc-branching in N-glycans, a phenotype that promotes growth arrest and inhibits autoimmunity by increasing surface retention of cytotoxic T lymphocyte antigen-4 (CTLA-4) via interactions with galectins. N-Acetylglucosaminyltransferase V (MGAT5) mediates beta1,6GlcNAc-branching by transferring N-acetylglucosamine (GlcNAc) from UDP-GlcNAc to N-glycan substrates produced by the sequential action of Golgi alpha1,2-mannosidase I (MIa,b,c), MGAT1, alpha1,2-mannosidase II (MII, IIx), and MGAT2. Here we report that TCR signaling enhances mRNA levels of MIa,b,c and MII,IIx in parallel with MGAT5, whereas limiting levels of MGAT1 and MGAT2. Blocking the increase in MI or MII enzyme activity induced by TCR signaling with deoxymannojirimycin or swainsonine, respectively, limits beta1,6GlcNAc-branching, suggesting that enhanced MI and MII activity are both required for this phenotype. MGAT1 and MGAT2 have an approximately 250- and approximately 20-fold higher affinity for UDP-GlcNAc than MGAT5, respectively, and increasing MGAT1 expression paradoxically inhibits beta1,6GlcNAc branching by limiting UDP-GlcNAc supply to MGAT5, suggesting that restricted changes in MGAT1 and MGAT2 mRNA levels in TCR-stimulated cells serves to enhance availability of UDP-GlcNAc to MGAT5. Together, these data suggest that TCR signaling differentially regulates multiple N-glycan-processing enzymes at the mRNA level to cooperatively promote beta1,6GlcNAc branching, and by extension, CTLA-4 surface expression, T cell growth arrest, and self-tolerance.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.